We’ve come to a point where we have now completed our discussion
of nephritic syndrome under glomerulonephritides.
So now, really, all that’s left is nephrotic, let’s take a look.
Nephrotic syndrome, your focus here should be on O representing protein, not just that,
also for the fact that it’s dealing with cytokines, not neutrophils.
Neutrophils will be the type of inflammation that we see with nephritic,
take the “itis” in nephritic and inflammation
and that to you should automatically bring you into the realm of neutrophils,
and that should be clear.
With nephrotic, an important difference here is the fact that you have cytokines that are involved
and this is a discussion that we had earlier
where well, we talked about children
and the most common cause of nephrotic syndrome in children
in fact is minimal change disease and doing the overview.
When I had talked about how T-cells then released cytokines
which then bring about the changes that we see in minimal change disease.
In case you missed that discussion, all we’re doing here is repeating it once more.
What do the cytokines do?
They will damage the podocytes in the certain conditions such as minimal change disease.
You will in fact have that fusion of the podocytes.
Before we move on, please conceptualize a picture of a podocyte
representing your visceral epithelial cell.
Next, because of cytokines, that all important negative charge
in your glomerular basement membrane has been lost,
so therefore, you further facilitate the release of or filtration of albumen.
Speaking of which, the protein that you’re losing here
will be greater than 3.5 grams of protein per day.
That’s rather significant so therefore, giving you a generalized pitting edema,
and this is due to hypoalbuminemia.
Next, now due to the risk of developing spontaneous peritonitis,
due to streptococcus type of pneumonia.
Keep that in mind please because of that and generalized edema,
there is an increased risk of developing that generalized tissue, spontaneous type of peritonitis.
Important clinical manifestations.
Now, it all begins with understanding nephrotic,
knowing that you’re losing quite a bit of protein,
in addition, you can have certain types that may present with hypertension.
So here, clinically, it’s important beyond the hypertension
to really understand what else is taking place in your patient.
Remember, I told you earlier,
whenever there’s damage to the kidney or to the glomerulus specifically,
that there’s every possibility that you might be retaining that sodium.
So let it be nephritic or nephrotic, you still may be retaining that sodium
so therefore, the manifestation here would be hypertension.
Now, what is a lot more specific for nephrotic versus nephritic is the hypercoagulability.
For nephrotic syndrome, the hypercoagulability will be due to the loss of antithrombin III.
Now, think about that for a second
because well, couldn’t you lose other coagulation factors resulting in a bleeding disorder?
Well, as much as that might be a possibility, really,
it’s making sure that you pay attention to your clinical presentation.
In a patient who’s losing tons of protein, has generalized edema,
and is hypercoagulable, that is your nephrotic syndrome, no doubt.
So what I’m saying is here, because of other physical attributes
or the attributes of charges and such that of all of the hemodynamic factors,
it will be antithrombin III that you’re losing.
Now, in order for you to make sense of this,
antithrombin III normally exists to what? Neutralize thrombin.
If you neutralize thrombin, how in the world are we supposed to then form a clot?
So normal functioning, normal functioning of antithrombin III is to neutralize thrombin.
What if you lose antithrombin III? What if you lose antithrombin III?
There’s nothing inhibiting thrombin formation.
So therefore, you’re going to then continue through the cascade and you end up forming a clot.
Welcome to hypercoaguability.
What else? Well, I’ve mentioned this a few times.
Whenever you have conditions in which protein is decreased,
you’ll find an inverse relationship or you then find lipid increasing.
In nephrotic syndrome, hypoalbuminemia, resulting in increase in cholesterol.
Now, there are many theories out there.
For right now, if I were you, clinically, you wanna memorize this as is it’s taking place.
So therefore, many of these conditions, we will find fatty casts and overall fat bodies.
Now, the hypogammaglobinemia is due to loss of gamma globulins in the urine.
And the fatty casts, maltese crosses, and fat bodies are obviously seen with nephrotic.
This is a key finding but keep in mind that relationship between
decreased protein for whatever reason, and increase in lipid profile.